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Development of Therapeutics for Heart Failure

The Management of Heart Failure

The Past, the Present, and the Future

Eugene Braunwald, MD

From the TIMI Study Group, Cardiovascular Division, Brigham and Women’s Hospital, Department of Medicine, Harvard Medical School, Boston, Mass.

Correspondence to Eugene Braunwald, MD, Chairman, TIMI Study Group, 350 Longwood Ave, Boston, MA 02115. E-mail ebraunwald@partners.org

Key Words: cells • gene therapy • genetics • heart failure

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
It is an honor to contribute to this inaugural issue of Circulation: Heart Failure and to provide some personal reflections on the management of heart failure (HF). I will comment on the past and the present and will venture to make some predictions about the future of this important subject.

	The Past

 
In 1950, as a medical student, I first learned about the management of congestive HF from the first edition of Harrison’s Principles of Internal Medicine,¹ which had just been published. Management consisted of strict bed rest, sedation, dietary sodium restriction, digitalis, venesection, and administration of morphine and mercurial diuretics; the latter were only modestly effective and were administered by painful intramuscular injection. All of these measures (other than mercurial diuretics) had not changed for about a half century.

I replaced Harrison as the cardiology editor of Harrison’s Principles of Internal Medicine for the sixth edition,² which was published in 1970. The management of HF, while still adhering to the principles set forth in the first edition, included 3 new aspects: (1) control of fluid retention with the (then) new orally effective diuretics—thiazides, the powerful new loop diuretics, as well as potassium-retaining diuretics (because of the widespread use of these agents, the adjective "congestive" was gradually eliminated from the name of the condition); (2) recognition and vigorous treatment of the precipitating causes of HF, such as infection, pulmonary embolism, and arrhythmias; and (3) intravenous dopamine, the powerful new β-adrenergic agonist for the management of acute, decompensated HF, including cardiogenic shock.

	The Present

 
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